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Biomedical subjects

M Ye

Publications and source records attributed to M Ye.

At least 109 records · Page 6Linked to original sources
PubMed1993

The secretion of fluid by renal cysts from patients with autosomal dominant polycystic kidney disease.

BACKGROUND: The mechanism by which fluid accumulates in renal cysts of adults with autosomal dominant polycystic kidney disease is not known. This study was designed to determine whether transepithelial secretion of fluid may account for this accumulation. METHODS: We studied in vitro intact cysts that were excised from kidneys removed from three patients with end-stage autosomal dominant polycystic kidney disease. The cysts were loaded with natural cyst fluid or with a combination of Dulbecco's modified Eagle's medium and Ham's F12 medium (DME-F12) and incubated in DME-F12 for 24 hours. Fluid secretion, determined by the change in the weight of the cysts, was expressed as the rate of fluid secretion per square centimeter of surface area per 24 hours, to correct for the wide variation in the sizes of the cysts. To test for endogenous secretagogues, cyst fluid was added to confluent monolayer cultures of canine- and human-kidney cells. RESULTS: During the first 24 hours of incubation, the mean (+/- SE) rate of fluid secretion in nine cysts containing natural cyst fluid was 20.8 +/- 5.6 microliters per square centimeter of surface area per 24 hours, as compared with 2.3 +/- 3.6 microliters per square centimeter per 24 hours in nine cysts containing incubation medium. Each group of cysts was then incubated with forskolin, a nonspecific stimulator of adenylate cyclase activity, for an additional 24 hours. During this period the fluid-secretion rate of cysts containing natural cyst fluid did not change; however, the secretion rate of those containing incubation medium increased to 9.1 +/- 4.4 microliters per square centimeter per 24 hours (mean change, 6.8 +/- 1.1; P < 0.001). Cyst fluid stimulated fluid secretion by polarized monolayers of canine- and human-kidney cells. CONCLUSIONS: Renal cysts from patients with autosomal dominant polycystic kidney disease can secrete fluid, and net fluid secretion can be increased by unidentified secretagogues in the cyst fluid. These results suggest that the process of cyst enlargement may be susceptible to pharmacologic intervention.

Cells, Cultured↗
PubMed1993

Cytosolic free calcium regulation in response to acute changes in intracellular pH in vascular smooth muscle.

This study examined the mechanisms whereby alterations of intracellular pH (pHi) impact on free cytosolic calcium (Cai2+) in cultured rat aortic vascular smooth muscle cells (VSMC) assayed in the presence of HCO3/CO2. Rapid cell alkalinization, effected by the exposure to NH4Cl or removal of CO2 from the superfusate, produced a rapid increase in Cai2+. The rise in Cai2+ was markedly diminished when sarcoplasmic reticulum (SR) Ca2+ stores had been depleted by prior exposure to arginine vasopressin (AVP) in Ca(2+)-free media or when SR release and reuptake of Ca2+ were blocked by the addition of 3,4,5-trimethoxybenzoic acid 8-(diethylamino)octyl ester (TMB-8), but was unaffected by the removal of external Ca2+ or inhibition of Ca2+ entry using NiCl2. Cell acidification also resulted in a rapid increase in Cai2+. This Cai2+ increase was most apparent when pHi was very low (< 6.6) and was unaffected by removal of external Ca2+ or NiCl2 addition. Unlike the effect of cell alkalinization, the increase in Cai2+ associated with cell acidification was not prevented by pretreatment with AVP or TMB-8. We conclude that, in cultured VSMC, acute intracellular alkalinization and, to a lesser extent, acidification result in release of Ca2+ from internal stores. Alkalinization increases Cai2+ by promoting its release from a store which is AVP and TMB-8 sensitive, most likely the SR. Cell acidification increases Cai2+ from an intracellular store(s) that is neither AVP nor TMB-8 sensitive. The increase in Cai2+ produced by cell acidification may be explained on the basis of cell buffering such that, as cytosolic H+ increases, it displaces Cai2+ from internal buffers with similar affinities for Ca2+ and H+.

Ammonium Chloride↗
PubMed1993

Function of the thyroarytenoid muscle in a canine laryngeal model.

Fundamental frequency is controlled by contraction of the thyroarytenoid (TA) and cricothyroid (CT) muscles. While activity of the CT muscle is known to tense and thin the vocal folds, little is known about the effect of the TA muscle on vocal fold vibration. An in vivo canine laryngeal model was used to examine the role of the TA muscle in controlling phonation. Isolated TA muscle activation was obtained by stimulating sectioned terminal TA branches through small thyroid cartilage windows. Subglottic pressure measures, electroglottographic and photoglottographic signals, and acoustic signals were obtained in 5 mongrel dogs during dynamic and static variations in TA muscle activity. Results indicated that TA muscle activation is a major determinant in sudden shifts from high-frequency to modal phonation. Subglottic pressure increased and open quotient decreased gradually with increasing TA activation.

Animals↗
PubMed1993

Function of the posterior cricoarytenoid muscle in phonation: in vivo laryngeal model.

The function of the posterior cricoarytenoid (PCA) muscle in phonation has not been well documented. To date, several electromyographic studies have suggested that the PCA muscle is not simply an abductor of the vocal folds, but also functions in phonation. This study used an in vivo canine laryngeal model to study the function of the PCA muscle. Subglottic pressure and electroglottographic, photoglottographic, and acoustic waveforms were gathered from five adult mongrel dogs under varying conditions of nerve stimulation. Subglottic pressure, fundamental frequency, sound intensity, and vocal efficiency decreased with increasing stimulation of the posterior branch of the recurrent laryngeal nerve. These results suggest that the PCA muscle not only acts to brace the larynx against the anterior pull of the adductor and cricothyroid muscles, but also functions inhibitorily in phonation by controlling the phonatory glottal width.

Animals↗
PubMed1993

Orthotopic laryngeal transplantation: is it time?

The notion of returning phonatory and respiratory function by transplanting larynges has fascinated and challenged the minds of laryngologists for many years. In the past, the problems of revascularization, tissue rejection, and physiologic vocal fold motion have stymied the success of research in this area. Today, advances in microvascular surgery, graft versus host response, and selective reinnervation have made laryngeal transplantation a theoretical, if not a practical reality. Despite this progress, serious ethical and fiscal considerations remain unresolved. This report will discuss these advances as well as concerns and will present the current UCLA laryngeal physiology laboratory experience with canine laryngeal transplantation.

Animals↗
PubMed1993

Determination of vocal fold mucosal wave velocity in an in vivo canine model.

The vocal fold traveling wave is essential to normal voice production. The present investigation examined whether the velocity of the traveling wave (TWV) could be consistently determined in an in vivo canine model and if traveling wave velocity is affected by changes in the amplitude of recurrent laryngeal nerve stimulation (RLNS) and superior laryngeal nerve stimulation (SLNS). The results showed that traveling wave velocity increased with an increase in recurrent laryngeal nerve stimulation at low constant superior laryngeal nerve stimulation, but was poorly correlated with increases in recurrent laryngeal nerve stimulation at a high level of superior laryngeal nerve stimulation. Furthermore, traveling wave velocity was significantly correlated with superior laryngeal nerve stimulation at constant recurrent laryngeal nerve stimulation. This study demonstrated the feasibility of objectively measuring traveling wave velocity in vivo.

Air↗
PubMed1992

The effect of pupil size on chromostereopsis and chromatic diplopia: interaction between the Stiles-Crawford effect and chromatic aberrations.

Several studies have reported that the magnitude of chromostereopsis changes as the pupil size changes. Einthoven's theory, that chromostereopsis is determined by interocular differences of monocular transverse chromatic aberration, can not easily explain this change. Therefore, several alternative hypotheses have been introduced, most notably by Vos [(1960) Vision Research, 6, 105-107], who argues that shifts in chromostereopsis with pupil size are due to decentration of the peak of the Stiles-Crawford effect (SCE) with respect to the pupil. We tested this hypothesis by measuring chromostereopsis under both scotopic (no SCE) and photopic conditions with centered and decentered artificial pupils. The results show that the SCE plays an important role in the effect of pupil size on chromostereopsis. Similar changes were also measured in monocular chromatic diplopia which supports the hypothesis that the effect of pupil size on chromostereopsis is due to monocular mechanisms.

Adult↗
PubMed1992

Involvement of multiple sulfhydryl groups in melatonin signal transduction in chick brain.

To gain insight into the molecular mechanism underlying melatonin binding and signal transduction in the chick brain, we have investigated the role of -SH groups, using a sulfhydryl alkylating reagent N-ethylmaleimide (NEM). At least two -SH groups are involved in the formation of the receptor-G protein complex: one is sensitive to and the other relatively insensitive to NEM. Alkylation of the sensitive group selectively abolishes high affinity binding of 2-[125I]iodomelatonin ([125I]MEL), similar to the effect induced by GTP, thus leading to a complete loss of sensitivity to nucleotides. Modification of both groups causes a marked reduction in binding capacity. Agonists with high affinity, but not other compounds with low affinity for the melatonin receptor, protect against alkylation by NEM. GTP gamma s does not significantly alter the reactivity of -SH groups towards NEM, but agonist-protected receptors remain sensitive to this nucleotide. Moreover, NEM pretreatment blocks the inhibitory effect of melatonin on forskolin-stimulated adenylate cyclase activity in chick brain. These data suggest that the -SH group modulating agonist affinity may lie within the coupling domain between the receptor and G protein but outside of the GTP binding site. In addition, sulfhydryl groups are essential for melatonin binding and signal transduction in chick brain.

Adenylyl Cyclases↗
PubMed1992

In vitro formation and expansion of cysts derived from human renal cortex epithelial cells.

Acquired renal cysts derive from terminally differentiated tubular epithelium in adults as a consequence of increased epithelial cell proliferation, fluid accumulation and extracellular matrix remodelling. To understand better how human epithelial cysts may be initiated and progressively expand, cells from primary cultures of normal human adult renal cortex were dispersed in polymerized type I collagen. The transparent matrix permitted repeated observation by light microscopy of cyst formation from individual renal cells. The cyst cells reacted strongly with distal nephron histochemical markers (cytokeratin antibodies AE1/AE3, epithelial membrane antigen, and Arachis hypogaea lectin) but inconsistently or not at all to markers of proximal tubules (Tetragonolobus purpureas lectin and Phaseolus vulgaris erthroagglutinin lectin). The number of spherical, fluid-filled epithelial cysts that developed in a standardized microscope field quantified cyst initiation. Cyst progression was determined from the increase in the diameter (surface area) of cysts and represents a hyperplastic event. EGF or TGF alpha, were required in serum-free defined medium to cause cysts to develop from individual epithelial cells dispersed in the matrix; insulin was required as a co-factor. The EC50 for EGF was approximately 0.1 ng/ml, and for insulin 1 microgram/ml. Early cultures of normal cortex formed cysts more efficiently when dispersed in collagen matrix than cells passaged several times before suspension in the gel. Agonists of adenylate cyclase (PGE1, AVP, VIP, PTH, forskolin, cholera toxin), methylisobutylxanthine, and 8-Br-cAMP, though incapable of causing cyst formation alone in defined medium, enhanced cyst initiation and progression in the presence of EGF and insulin. Angiotensin II, TNF alpha, beta-estradiol, and pertussis toxin had no effect in the absence or presence of EGF and insulin. Pertussis toxin inhibited cyst initiation and expansion caused by EGF and forskolin but potentiated cyst initiation and expansion caused by EGF and PGE1. Cyst formation and expansion were inhibited by TGF beta 1 and 2-chloroadenosine. Polarized monolayers of human renal cortical cells grown on permeable membranes were used to independently quantify the effects of agonists on the net secretion of solute and water from the basolateral to the apical surface of the cells. PGE1, forskolin, and 8-Br-cAMP stimulated net fluid secretion that was sustained for several days; EGF enhanced forskolin-stimulated fluid secretion. We conclude that the formation and expansion of in vitro cysts derived from solitary human cortex cells depends on the coordinated interplay between cellular proliferation and fluid secretion.(ABSTRACT TRUNCATED AT 400 WORDS)

Body Fluids↗
PubMed1992

Chromatic aberration and optical power of a diffractive bifocal contact lens.

Although diffractive contact lenses have been well documented in theory, no definitive experimental data have been reported which confirm that the near image is in fact created by diffraction rather than by refraction. We have tested the diffraction hypothesis for one type of diffractive contact lens (the Hydron Echelon bifocal) experimentally by measuring its longitudinal chromatic aberration in isolation and when worn on the eye. The basis of this test is that, according to theory, diffractive lenses should have chromatic aberration which is opposite in sign to that measured for the eye. Objective measurements of chromatic aberration were made with a focimeter when the lens was in a wet cell. Subjective measurements were made with a Badal optometer when the lens was worn on the eye. Four control experiments were conducted to provide baseline measurements of the eye's chromatic aberration, against which we compared the results obtained for the diffractive contact lens. The data were also compared with conventional measurements of refractive error obtained by standard subjective techniques and by an automated infrared refractor. Our results showed that the longitudinal chromatic aberration of the diffraction image of the Echelon bifocal lens was about one-half that obtained under the four control conditions: for the naked eye, for the nondiffraction image of the Echelon lens, or for either image of a refractive bifocal contact lens (CIBA Bisoft). These results are consistent with the theoretical prediction that the negative chromatic aberration of a diffractive contact lens should partially cancel the positive chromatic aberration of the human eye.(ABSTRACT TRUNCATED AT 250 WORDS)

Color Perception↗
PubMed1992

Cyst fluid from human autosomal dominant polycystic kidneys promotes cyst formation and expansion by renal epithelial cells in vitro.

Autosomal dominant polycystic kidney disease (ADPKD) is characterized by progressive renal enlargement, culminating in renal insufficiency in over one half of affected individuals. The highly variable onset and clinical course of ADPKD may be due to factors extrinsic to the genetically defined renal cysts. In this study, cyst fluid samples from 12 nonazotemic and 18 azotemic ADPKD subjects were examined for in vitro biologic activity that promotes cellular proliferation and the secretion of fluid by renal epithelial monolayers, two pathogenetic mechanisms that have critical roles in the formation and the rate of expansion of renal cysts. Cyst fluid added to culture medium (final concentrations, 1 to 20%) caused Madin-Darby canine kidney cells and human kidney cortex (HKC) cells derived from primary cultures to form cysts in Type I collagen matrix. Cyst fluid stimulated the net transepithelial secretion of fluid by polarized monolayers composed of these same cells. Absolute levels of fluid secretory activity determined by MDCK bioassay were correlated directly with the rate of fluid secretion by HKC cell monolayers and with the extent of cyst formation by MDCK and HKC cells embedded in collagen matrix. The secretory activity of urine was negligible; secretory activity was detectable in the serum of normal and ADPKD subjects, but the levels were much lower than in cyst fluid. cAMP agonists prostaglandins E1 and E2, arginine vasopressin, and 8-Br-cAMP stimulated fluid secretion by MDCK and HKC monolayers, but these substances did not cause HKC cells to form cysts in collagen matrix, whereas cyst fluid did. Among other naturally occurring growth factors and autacoids, only epidermal growth factor and transforming growth factor alpha stimulated cyst formation by HKC cells; however, the capacity of cyst fluid to stimulate fluid secretion was not affected by treatment with antiserum to epidermal growth factor. It was concluded that potent, and possibly unique, substances in the cyst fluids of individuals with ADPKD support and augment biologic processes in renal epithelial cells that may be important in the promotion of progressive cyst expansion.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1992

The establishment of rat-mouse hybridomas secreting anti-aflatoxin M1 antibodies and the properties of their monoclonal antibodies.

After a comparison of anti-AFM1-BSA antibody responses between rat and mouse, the spleen cells of rat with stronger responses were chosen as parent cells for fusing with mouse myeloma cells P3X63-Ag8.653. Through HAT medium selection, RIA screening and cloning, five well growing rat-mouse hybridoma clones were obtained that could secret anti-AFM1 antibodies stably. The results from ELISA and competitive binding RIA further proved that the 5 McAbs are direct against AFM1, with significant cross reaction to its derivative, AFB1. The average affinity constant of the 5 McAbs is 10(9)-10(11) l/M. It signifies that these monoclonals have potential application value for the construction of AF detection kit.

Aflatoxin M1↗
PubMed1992

[Bacterial microcolony and its primary applications].

A new rapid and useful microcolony technique was developed by using cellulose-acetate membrane as a supporter. The bacteria were inoculated on the membrane and cultivated for 3-6h. Then the membrane was rendered, fixed and colored. The microcolonies were observed and counted under the microscope. By using this technique the microcolonies of 139 strains of bacteria were observed. 72 strains of Staphylococcus were differentiated by means of observing the characteristics of the microcolonies. The correlation rate between the microcolony method and the routine method was 90.28%. This technique was also first used to determine the bacteria numbers in urine within 6h, and the advantages of it were significant compared with the plate count method.

Colony Count, Microbial↗
PubMed1991

Pertussis toxin blocks melatonin-induced inhibition of forskolin-stimulated adenylate cyclase activity in the chick brain.

The high-affinity guanine nucleotide-sensitive receptor sites for melatonin in the mammalian hypothalamus and pars tuberalis mediate inhibition of adenylate cyclase (AC) activity. Therefore, we have examined whether similar sites in the chick brain and retina also modulate AC activity. Melatonin did not alter basal or forskolin-stimulated AC activity in whole forebrain or retinal homogenates. In contrast, melatonin significantly inhibited forskolin-stimulated AC activity in forebrain synaptosomal membranes and partially purified retinal membranes in a concentration-dependent manner. Maximal inhibition (approximately 25-30%) of stimulated AC activity was observed at 10-100nM melatonin, while the concentrations (EC50's) which caused half-maximal effects were 22 +/- 6 pM and 30 +/- 5 pM in the brain and retina respectively. Pretreatment of forebrain slices with pertussis toxin abolished the inhibitory effect of melatonin on stimulated AC activity. These data provide the first evidence that melatonin suppresses AC activity in the chick CNS via a pertussis toxin-sensitive G-protein.

Adenylate Cyclase Toxin↗
PubMed1991

Interocular differences in transverse chromatic aberration determine chromostereopsis for small pupils.

Chromostereopsis has been attributed previously to interocular differences in foveal transverse chromatic aberration (TCA). We tested this hypothesis by measuring chromostereopsis as a function of the separation of small artificial pupils. We also measured the monocular transverse chromatic aberration under the same conditions. Our results show that chromostereopsis with small pupils can be precisely accounted for by the interocular difference in monocular transverse chromatic aberration. This relationship is closely predicted by a simple water eye model.

Color Perception↗